Vitamin D and kidney disease

Calcium and phosphorus are essential minerals required for many critical biologic functions including cell signaling, energy metabolism, skeletal growth and integrity. Calcium and phosphate homeostasis are maintained primarily by regulation of epithelial calcium and phosphate cotransport in the kidn...

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Main Authors: Lisa Keung, Farzana Perwad
Format: Article
Language:English
Published: Elsevier 2018-12-01
Series:Bone Reports
Online Access:http://www.sciencedirect.com/science/article/pii/S2352187218300433
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spelling doaj-a2400719249144ebb71c970e5650e5ef2020-11-25T00:13:23ZengElsevierBone Reports2352-18722018-12-01993100Vitamin D and kidney diseaseLisa Keung0Farzana Perwad1University of California San Francisco, San Francisco, CA, United StatesCorresponding author.; University of California San Francisco, San Francisco, CA, United StatesCalcium and phosphorus are essential minerals required for many critical biologic functions including cell signaling, energy metabolism, skeletal growth and integrity. Calcium and phosphate homeostasis are maintained primarily by regulation of epithelial calcium and phosphate cotransport in the kidney and intestine, processes that are tightly regulated by hormones including 1,25 dihydroxyvitamin D (1,25(OH)2D), fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH). In patients with chronic kidney disease (CKD), as renal function declines, disruption of feedback loops between these hormones have adverse consequences on several organ systems, including the skeleton, heart and vascular system. CKD-associated mineral and bone disorder (CKD-MBD) is defined as a systemic disorder of mineral and bone metabolism due to CKD manifested by abnormalities of calcium, phosphorus, PTH or vitamin D metabolism, abnormalities of bone turnover, mineralization and volume, and ectopic soft tissue calcification. Complications of CKD-MBD include vascular calcification, stroke, skeletal fracture and increased risk of death. Increased FGF23 and PTH concentrations, and 1,25(OH)2D deficiency contribute to the pathogenesis of CKD-MBD. Therefore, treatment of patients with CKD-MBD is focused on restoring the feedback loops to maintain normal calcium and phosphate balance to prevent skeletal and cardiovascular complications. Keywords: Calcium, Vitamin D, Parathyroid hormone (PTH), Parathyroid hormone related protein (PTHrP), Kidneyhttp://www.sciencedirect.com/science/article/pii/S2352187218300433
collection DOAJ
language English
format Article
sources DOAJ
author Lisa Keung
Farzana Perwad
spellingShingle Lisa Keung
Farzana Perwad
Vitamin D and kidney disease
Bone Reports
author_facet Lisa Keung
Farzana Perwad
author_sort Lisa Keung
title Vitamin D and kidney disease
title_short Vitamin D and kidney disease
title_full Vitamin D and kidney disease
title_fullStr Vitamin D and kidney disease
title_full_unstemmed Vitamin D and kidney disease
title_sort vitamin d and kidney disease
publisher Elsevier
series Bone Reports
issn 2352-1872
publishDate 2018-12-01
description Calcium and phosphorus are essential minerals required for many critical biologic functions including cell signaling, energy metabolism, skeletal growth and integrity. Calcium and phosphate homeostasis are maintained primarily by regulation of epithelial calcium and phosphate cotransport in the kidney and intestine, processes that are tightly regulated by hormones including 1,25 dihydroxyvitamin D (1,25(OH)2D), fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH). In patients with chronic kidney disease (CKD), as renal function declines, disruption of feedback loops between these hormones have adverse consequences on several organ systems, including the skeleton, heart and vascular system. CKD-associated mineral and bone disorder (CKD-MBD) is defined as a systemic disorder of mineral and bone metabolism due to CKD manifested by abnormalities of calcium, phosphorus, PTH or vitamin D metabolism, abnormalities of bone turnover, mineralization and volume, and ectopic soft tissue calcification. Complications of CKD-MBD include vascular calcification, stroke, skeletal fracture and increased risk of death. Increased FGF23 and PTH concentrations, and 1,25(OH)2D deficiency contribute to the pathogenesis of CKD-MBD. Therefore, treatment of patients with CKD-MBD is focused on restoring the feedback loops to maintain normal calcium and phosphate balance to prevent skeletal and cardiovascular complications. Keywords: Calcium, Vitamin D, Parathyroid hormone (PTH), Parathyroid hormone related protein (PTHrP), Kidney
url http://www.sciencedirect.com/science/article/pii/S2352187218300433
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